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Government-Owned Inventions; Availability for Licensing

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AGENCY:

National Institutes of Health, Public Health Service, HHS.

ACTION:

Notice.

SUMMARY:

The inventions listed below are owned by an agency of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing.

ADDRESSES:

Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301-496-7057; fax: 301-402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

CDK4-Transformed Mouse Podocytes Useful for Studying Glomerular Diseases

Description of Technology: Podocytes, cells of the visceral epithelium in the kidneys, are a key component of the glomerular filtration barrier. Podocyte damage and loss contribute to the initiation of glomerular diseases. Cyclin-dependent kinase 4 (CDK4), a catalytic subunit of the cyclin D-CDK4 serine/threonine kinase complex, is a critical regulator of the cell cycle. Recent studies showed that cells immortalized with CDK4 are useful to study pathophysiology. NIH investigators have generated mouse podocytes transformed with CDK4 as a nonviral immortalizing gene. These transformed podocytes show podocyte characteristics and express podocyte markers. Furthermore, confluent CDK4-podocyte cultures show higher levels of gene expression for multiple podocyte differentiation genes compared with subconfluent or lower density culture.

Development Stage:

  • Early-stage.
  • Pre-clinical.
  • In vitro data available.

Potential Commercial Applications:

  • Model system for study of glomerular disorders.
  • Useful tools to study podocyte biology.

Competitive Advantage: Better model system to study podocyte structure and function.

Inventors: Drs. Toru Sakairi and Jeffrey B. Kopp (NIDDK).

Publication: Sakairi T, et al. Cell-cell contact regulates gene expression in CDK4-transformed mouse podocytes. Am J Physiol Renal Physiol. 2010 Oct;299(4):F802-809. [PMID: 20668098].

Intellectual Property: HHS Reference No. E-287-2010/0—Research Tool (Materials available for licensing: CDK4 podocytes). Patent protection is not being pursued for this technology.

Related Technology: HHS Reference No. E-049-2007/0—Model for Study of Glomerular Disorders: Conditionally-Immortalized Mouse Podocyte Cell Line with Tet-on-Regulated Gene Expression (Dr. Jefferey B. Kopp, NIDDK).

Licensing Contact: Suryanarayana (Sury) Vepa, PhD; 301-435-5020; vepas@mail.nih.gov.

Conditionally Immortalized Human Podocyte Cell Lines

Description of Technology: Podocytes, cells of the visceral epithelium in the kidneys, are a key component of the glomerular filtration barrier. Podocyte damage and loss contribute to the initiation of glomerular diseases. NIH investigators recently established long-term urinary cell cultures from two patients with focal segmental glomerulosclerosis and two healthy volunteers, via transformation with the thermosensitive SV40 large T antigen (U19tsA58) together with human telomerase (hTERT). Characterization of randomly selected clonal cell lines from each human subject showed mRNA expression for the podocyte markers synaptopodin, nestin, and CD2AP in all clones. Podocin mRNA was absent from all clones. The expression of nephrin, Wilms tumor 1 (WT1), and podocalyxin mRNA varied among the clones, which may be due to transformation and/or cloning. These novel human urine-derived podocyte-like epithelial cell lines (HUPECs) generated from urine of patients and healthy volunteers will be useful to study podocyte cell biology.

Development Stage:

  • Early-stage.
  • Pre-clinical.
  • In vitro data available.

Potential Commercial Applications:

  • Model system for study of glomerular disorders.
  • Useful tools to study podocyte biology.

Competitive Advantage: These podocyte-like cells are unique and novel compared to the currently available podocyte cells because these are obtained from individuals with glomerular disease.

Inventors: Drs. Toru Sakairi and Jeffrey B. Kopp (NIDDK).

Publication: Sakairi T, et al. Conditionally immortalized human podocyte cell lines established from urine. Am J Physiol Renal Physiol. 2010 Mar;298(3):F557-67. [PMID: 19955187]

Intellectual Property: HHS Reference No. E-252-2010/0—Research Tool. Patent protection is not being pursued for this technology.

Related Technologies:

  • HHS Reference No. E-049-2007/0—Model for Study of Glomerular Disorders: Conditionally-Immortalized Mouse Podocyte Cell Line with Tet-on-Regulated Gene Expression (Dr. Jefferey B. Kopp, NIDDK).
  • HHS Reference No. E-287-2010/0—CDK4-Transformed Mouse Podocytes Useful for Studying Glomerular Diseases (Drs. Toru Sakairi and Jeffrey B. Kopp, NIDDK)

Licensing Contact: Suryanarayana (Sury) Vepa, PhD; 301-435-5020; vepas@mail.nih.gov.

An In-Vitro Cell System Useful For Identification of RORγ Antagonists

Description of Technology: The retinoid-related orphan receptors alpha, beta and gamma (RORα, β and γ, also referred to as NR1F1, 2 and 3, respectively) comprise a distinct subfamily of nuclear receptors. Study of ROR-deficient mice has implicated RORs in the regulation of a number of biological processes and revealed potential roles for these proteins in several pathologies. NIH investigators have developed an in-vitro system using CHO cells stably expressing a TET-On expression vector regulating RORγ and a RORE-Luciferase reporter. This system Start Printed Page 47218allows inducible expression of RORγ upon addition of doxycycline. Upon its induction RORγ binds to the RORE in the luciferase reporter plasmid and induces luciferase. This system can be used to identify RORγ antagonists. This system has been tested successfully in 1536-well plate high throughput analysis.

Potential Commercial Applications: Identification of therapeutic compounds to treat asthma, inflammation, and various autoimmune diseases such as osteoarthritis, multiple sclerosis.

Competitive Advantages: Novel and unique system to screen and identify chemical and drugs for their RORγ antagonistic activity.

Development Stage:

  • Early-stage.
  • Pre-clinical.
  • In vitro data available.

Inventors: Drs. Yukimasa Takeda and Anton M. Jetten (NIEHS).

Publications:

1. Jetten AM. Retinoid-related receptors (RORs): Critical roles in development, immunity, circadian rhythm, and cellular metabolism. Nucl Recept Signal. 2009;7:1-32. [PMID: 19381306].

2. Yang XO, et al. T helper 17 lineage differentiation is programmed by orphan receptors ROR alpha and ROR gamma. Immunity 2008 Jan;28(1):29-39. [PMID: 18164222].

3. Kurebayashi S, et al. Retinoid-related orphan receptor gamma (RORgamma) is essential for lymphoid organogenesis and controls apoptosis during thymopoiesis. Proc Natl Acad Sci USA. 2000 Aug 29;97(18):10132-10137. [PMID:10963675].

Intellectual Property: HHS Reference No. 253-2010/0—Research Tool. Patent protection is not being pursued for this technology.

Related Technology: HHS Reference No. E-222-2009/0—RORgamma (RORC) Deficient Mice Which Are Useful for the Study of Lymph Node Organogenesis and Immune Responses (Dr. Anton M. Jetten, NIEHS).

Licensing Contact: Suryanarayana (Sury) Vepa, PhD; 301-435-5020; vepas@mail.nih.gov.

Collaborative Research Opportunity: The NIEHS, Laboratory of Respiratory Biology, Cell Biology Group, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize retinoid-related orphan receptors (RORs) function in chronic diseases. For collaboration opportunities, please contact Elizabeth M. Denholm, PhD at denholme@niehs.nih.gov.

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Dated: July 27, 2011.

Richard U. Rodriguez,

Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.

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[FR Doc. 2011-19817 Filed 8-3-11; 8:45 am]

BILLING CODE 4140-01-P